11. Glomerular Pathology Flashcards
Where is the likely site of injury in proteinuria/nephrotic syndrome?
Podocyte or subepithelial damage.
What are the 3 most common primary causes of proteinuria/nephrotic syndrome?
Minimal change glomerulonephritis.
Focal segmental glomerulosclerosis.
Membranous glomerulonephritis.
Name 1 common secondary cause of proteinuria/nephrotic syndrome?
Diabetes mellitus.
Amyloidosis.
Which age group is minimal change glomerulonephritis most common in?
Childhood/adolescence.
What treatment does minimal change glomerulonephritis respond to?
Steroids (but may recur when steroids stopped).
Does minimal change glomerulonephritis usually progress to renal failure?
No, does not usually progress to renal failure.
How does the glomerulus look histologically in minimal change glomerulonephritis?
Glomerulus looks normal, but there are no podocytes visible as they have been damaged (cannot selectively filter proteins anymore).
What causes podocyte damage in minimal change glomerulonephritis?
An unknown circulating factor damages the podocytes. There is no immune complex deposition.
In which age group is focal segmental glomerulosclerosis more common?
Adults.
What causes podocyte damage in focal segmental glomerulosclerosis and what consequence does this have for treatment?
Circulating factor damages podocytes. FSGS is progressive to renal failure, but if the patient has a kidney transplant, the transplanted kidney will also get FSGS due to the circulating factors. So treatment is with dialysis rather than transplant.
Which age group if membranous glomerulonephritis most common in?
Adults.
How does membranous glomerulonephritis typically progress?
1/3 patients get better.
1/3 patients continue as they are.
1/3 patients progress to renal failure.
What causes podocyte damage in membranous glomerulonephritis?
Immune complex deposits against the podocytes - sub-epithelial deposits (so is probably autoimmune).
Is membranous glomerulonephritis primary or secondary?
Is primary but may be secondary as has been associated with other pathologies eg lymphoma.
What is seen histologically in patients with diabetes mellitus leading to nephrotic syndrome?
Mesangial sclerosis leading to nodules.
Basement membrane thickening.
Does nephrotic syndrome secondary to diabetes mellitus progress to renal failure?
Yes - progressive proteinuria and is progressive to renal failure.
What are the two most common causes of haematuria?
IgA nephropathy.
Thin glomerular basement membrane disease/hereditary nephropathy (Alport).
What are the two most common causes of nephritic syndrome?
Goodpasture syndrome (anti-GBM disease). Vasculitis.
In which age group os IgA nephropathy most common?
Any age group.
What type of infections is IgA nephropathy associated with?
Mucosal infections - viral upper respiratory tract eg common cold.
Does IgA nephropathy present with proteinuria?
It can present with or without proteinuria.
Does IgA nephropathy progress to renal failure?
A significant proportion progress to renal failure.
How would you treat a patient with IgA nephropathy?
There is no effective treatment.
What is mesangial damage? Why does this occur and how does this lead to haematuria.
Loss of mesangial cells in the glomerulus.
Immune complexes (IgA) pass though the glomerulus to the mesangial cells causing damage.
Capillary loop becomes fragile, leading to haematuria.
Name 2 heredity nephropathies that do not progress to renal failure.
Thin GBM nephropathy.
Benign familial nephropathy.
Isolated haematuria.
Thin GBM.
Name 2 hereditary nephropathies that can progress to renal failure.
Alport. X linked. Abnormal collagen IV. Associated with deafness. Abnormal appearing GBM.
Are hereditary nephropathies as clear cut as either progressive to renal failure or not progressive?
No, often a grey area of patients between the two types of conditions, likely to be because multiple genes make up the conditions.
What is seen histologically in the glomerulus of patients with Alport’s syndrome?
Abnormally split and laminated GBM.
Does goodpasture syndrome (anti-GBM) progress to renal failure?
Yes, is very rapidly progressive.
How does goodpasture syndrome usually present?
Acute onset of severe nephritic syndrome, classically associated with pulmonary haemorrhage (smokers).
What causes GBM damage in goodpasture syndrome?
Autoantibody to collage IV in basement membrane. IgG deposition, inflammation and necrosis, filter blocked, becomes nephritic and blood leaks out.
How would you treat goodpasture syndrome if it is caught early?
Immunosuppresion and plasmaphoresis.
What causes GBM damage in vasculitis?
Anti neutrophil cytoplasmic antibodies and neutrophils cause segmental necrosis by activating complement and so punching out holes in the GBM - endothelial damage.
Is there immune complex/antibody deposition in vasculitis?
No - circulating antibodies to white cells.
Is vasculitis treatable? What do you need to do urgently if you suspect a patient has vasculitis?
Only if caught early.
Urgent biopsy.
How do patients with nephritic syndrome tend to present?
Hypertension.
Haematuria.
Oliguria.
Glomerular inflammation and reduction in GFR.
How do patients with nephrotic syndrome tend to present?
Hypoalbuminemia.
Hyperlipidaemia.
Proteinuria.
Peripheral oedema.
What conditions can present as either nephritic or nephrotic syndrome?
IgA purpura.
Post-infectious.
Lupus.
How do patients with vasculitis tend to present?
Systemic symptoms - lungs affected (pulmonary-renal syndrome), fatigue, arthralgia, myalgia, weight loss.
